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PEER
REVIEWED
72
FOCUS ON
virus, peste des petits ruminants virus, phocine
distemper virus, CDV, dolphin morbillivirus, porpoise
morbillivirus, equine morbillivirus (Hendra virus), and
porcine morbillivirus (Menangle virus)
6
—the primary
cause of distemper in ferrets is infection with CDV.
8
EPIDEMIOLOGY
Several outbreaks of CDV infections in ferrets have
been documented throughout the world over the past
10 years. In an outbreak of distemper in Spain in 2006,
14 domestic ferrets died.
4
Three confirmed cases of CDV
infections in ferrets that were euthanized in 2006, 2012,
and 2013 were reported in New South Wales and the
Australian Capital Territory.
1
Two cases of distemper in
domestic ferrets were reported in Germany in 2006.
10
A
major outbreak of distemper was reported in Denmark
in 2012. Danish farmed mink (Neovison vison) were
mainly affected. In a study of this outbreak, Trebbien
showed that carnivores (foxes, raccoons, dogs, and
ferrets) in that area affected by the disease died of CDV,
showing an identity at the nucleotide level of 99.45%
to 100%.
9
In the United States, free-ranging raccoons
(Procyon lotor) are the main species affected by CDV in
wildlife, serving as a potential disease reservoir.
3
A large
outbreak of distemper in raccoons living around a large
suburban zoo in the United States was reported in 2001.
11
PATHOGENESIS
Infections caused by a morbillivirus are spread by aerosol
transmission and show a highly contagious pattern.
Contact with exudates (eg, conjunctival and nasal), urine,
feces, and skin is often a source of transmission. The virus
shows a strong affinity for epithelial cells and lymphoid
tissue of the upper respiratory tract. This is where
the first phase of viral replication occurs.
6
Clinically,
this phase is observed 3 to 6 days after infection. It is
characterized by lymphopenia and pyrexia. The patient
has viremia at this point, resulting in systemic infection
of the lymphatic tissue. There is a strong correlation of
immunosuppression and virulence. The fever is biphasic
and recurs in the second phase of viremia a few days
later. The systemic infection of the epithelial cells severely
affects the patient, resulting in damage to the mucosal
tissue. At this stage, patients show serous nasal discharge,
conjunctivitis, and anorexia, clinically resembling an
influenza infection ( FIGURE 2 ). Dermatologic signs,
including facial and perineal dermatitis, as well as
dermatitis on the abdomen, completely resolve between
17 and 22 days after infection.
12
The entire respiratory
and gastrointestinal tract can be severely affected, and
disturbance of the epithelial cell layer predisposes patients
to secondary bacterial infections.
6
Because of the clinical
resemblance to influenza infectious, it is important to
diagnose distemper early to avoid potential shedding of
the virus and potential contamination of the clinic.
Neurologic signs resulting from acute encephalomyelitis
have been described but are not always present in
affected animals. Of note, during the previously
mentioned 2006 outbreak in Spain, none of the affected
animals showed any neurologic signs.
4
Depending
on the strain of the virus, patients may be moribund
after 16 days of infection, a condition that justifies
humane euthanasia or results in death. Dermatologic
signs, such as hyperkeratosis of footpads or the nasal
plane, as observed in canines, are rare
12
( FIGURE 3 ).
FIGURE 2. The catarrhal phase of CDV involves anorexia,
pyrexia, photosensitivity, and serous nasal discharge.
Mucopurulent ocular and nasal discharge with possible
bacterial pneumonia may be seen with a secondary
bacterial infection, which resembles an influenza infection.
Photo courtesy of Dr. Jeff Baier
FIGURE 3. The hard pad lesions on affected ferrets are
usually not as pronounced as those on dogs, most likely
because of the rapid progression of the disease. Photo
courtesy of Dr. Jeff Baier